Acute myocardial infarction (AMI), which represents the main public health issue around the world. Pro-angiogenesis has become one of the treatment methods for AMI. Studies have shown that mir-133a plays an important role in the angiogenesis process of AMI patients, but its mechanism is not clear.We hope to investigate the mechanism of mir-133a-induced damage to human umbilical vein endothelial cells (HUVECs) by transcriptome analysis, and explore its potential as a novel diagnostic and therapeutic target of AMI.RTq-PCR was used to detect the expression of miR-133a in peripheral blood of AMI patients and normal people. Mir133a over-expression promoted proliferation and migration ability of HUVEC.Transcriptome data was subsequently analyzed by a series of the bioinformatic approaches.GSEA enrichment analysis revealed 9 pathways with the most significant differences, two of which were the NF-κB signaling pathway and NOD-like receptor signaling pathway, both of them were closely associated with AMI. In addition, CXC8/IL1β genes were identified as the key hub genes covering the two pathways.The data of this study reveals that abnormal expression of miR-133a may cause endothelial injury. The potential mechanism is that miR-133a causes abnormalities of NF-κβ signaling pathway and NOD-like receptor signaling pathway. In particular, the two genes CXC8/IL1β are down-regulated by miR-133a.This indicates the potential of miR-133a as a diagnostic biomarker and molecular target to improve the treatment of AMI.